The results presented in this paper dissect the importance of this process, applying pharmacological inhibitors, precise removal or deliberate over expression of lively Akt in SKOV 3 ovarian cancer cell migration and invasion with respect to regulation of PAI 1 and uPA expression. The PI3K pathway is associated with many cellular processes, including proliferation, emergency, apoptosis, migration, invasion and cytoskeletal rearrangements. The harmony between PAI 1 and uPA expression is gentle, but vitally important in controlling cell behavior. A shift in PFT �� the balance towards PAI 1, whether due to an increase in PAI 1, a reduction in uPA or a mixture of both, has a tendency to avoid in-vitro migration and invasion of cancer cells, as we and others have shown previously. Furthermore, down-regulation of PAI 1, up regulation of uPA or both would shift the balance in favor of uPA and presumably upsurge in vitro migration and invasion. This concept helps to explain our results utilizing a survey of pharmacological inhibitors to signaling pathways known to affect cell migration. No matter the change in PAI 1 expression, the inhibitors of Rho kinase/ROCK, p38 MAPK, MEK and PI3K all decrease uPA expression in SKOV3 ovarian cancer cells, effectively shifting the PAI 1:uPA balance in favor of PAI 1. Just the p38 MAPK, MEK and PI3K inhibitors decrease injury caused SKOV 3 cell migration. The lack of effect of Cholangiocarcinoma the Rho kinase/ROCK inhibitor may be due to only a small reduction in uPA phrase. Collectively, our results support the finding that various signaling pathways positively and negatively modify equally uPA phrase and PAI 1 to seriously control SKOV 3 cell injury induced migration. Through our studies, a new link emerges between PAI1 expression and levels of phosphorylated Akt, which alters both cell migration and cell invasion. SKOV 3 cells treated with LY294002 showed a dependent decrease in phosphorylated Akt, a dependent increase in PAI 1 and a decrease in uPA. Inhibition of PI3K exercise also resulted in a dependent decrease in invasion and cell migration in a ATP-competitive ALK inhibitor assay, and a dependent decrease in migration tested in an injury caused migration assay. Like-wise, particular down-regulation of Akt by siRNA resulted in a in uPA expression, an increase in PAI 1 expression and a decrease in injury stimulated migration. By comparison, expression of constitutively active Akt caused the contrary effects on SKOV 3 cells: an in phosphorylated Akt levels correlated with a in PAI 1 expression and an increase in wound stimulated migration. The improvements in SKOV 3 cell migration that accompanied the increase o-r decrease in active Akt levels were similar to previously published reports.